Transcript DEFINITIONS OF PREGNANCY-RELATED HYPERTENSIVE

Preeclampsia
Eclampsia
uptodate 2014
There are four major hypertensive disorders related to
pregnancy
 Preeclampsia
Eclampsia
HELLP syndrome (Hemolysis, Elevated Liver enzymes, Low Platelets) HELLP may be an
independent disorder. As many as 15 to 20 percent of affected patients do not have concurrent
hypertension or proteinuria, leading some experts to believe that HELLP syndrome is a
separate disorder from preeclampsia
 Chronic/preexisting hypertension
Chronic/preexisting hypertension is defined as systolic pressure ≥140 mmHg and/or
diastolic pressure ≥90 mmHg that antedates pregnancy or is present before the 20th week
of pregnancy (on at least two occasions) or persists longer than 12 weeks postpartum
 Preeclampsia superimposed upon chronic/preexisting hypertension
 Gestational hypertension
During pregnancy, gestational hypertension refers to hypertension without proteinuria or
other signs/symptoms of preeclampsia that develops after 20 weeks of gestation .it should
resolve by 12 weeks postpartum.
DEFINITIONS OF PREGNANCYRELATED HYPERTENSIVE DISORDERS
Preeclampsia is a multi-system disorder characterized by the
new onset of hypertension and either proteinuria or end-organ
dysfunction in the last half of pregnancy .Although most affected
pregnancies deliver at term or near term with good maternal
and fetal outcomes, these pregnancies are at increased risk for
maternal and/or fetal mortality or serious morbidity
Criteria for the diagnosis of preeclampsia
Systolic blood pressure ≥140 mmHg or diastolic blood pressure ≥90
mmHg on two occasions at least four hours apart after 20 weeks of
gestation in a previously normotensive patient
and
Proteinuria ≥0.3 grams in a 24-hour urine specimen or
protein (mg/dL)/creatinine (mg/dL) ratio ≥0.3
Dipstick 1+ if a quantitative measurement is unavailable
In patients with new-onset hypertension without proteinuria, the new
onset of any of the following is diagnostic of preeclampsia:
Platelet count <100,000/microliter
Serum creatinine >1.1 mg/dL or doubling of serum creatinine in the
absence of other renal disease
Liver transaminases at least twice the normal concentrations
Pulmonary edema
Cerebral or visual symptoms
.
The presence of one or more of the following indicates a
diagnosis of "preeclampsia with severe features"
Symptoms of central nervous system dysfunction:
•New onset cerebral or visual disturbance, such as:
Photopsia, scotomata, cortical blindness, retinal vasospasm
•Severe headache (ie, incapacitating, "the worst headache I've ever had") or headache
that persists and progresses despite analgesic therapy
•Altered mental status
Hepatic abnormality:
Severe persistent right upper quadrant or epigastric pain unresponsive to medication and
not accounted for by an alternative diagnosis or serum transaminase concentration ≥
twice normal, or both
The presence of one or more of the following indicates a
diagnosis of "preeclampsia with severe features"
• Severe blood pressure elevation:
Systolic blood pressure ≥160 mmHg or diastolic blood pressure ≥110
mmHg on two occasions at least four hours apart while the patient is on
bedrest (unless the patient is on antihypertensive therapy)
• Thrombocytopenia:<100,000 platelets/microL
• Renal abnormality:
Progressive renal insufficiency (serum creatinine >1.1 mg/dL or doubling
of serum creatinine concentration in the absence of other renal disease)
• Pulmonary edema
•
In 2013, the American College of Obstetricians and
Gynecologists removed proteinuria as an essential
criterion for diagnosis of preeclampsia. They also
removed massive proteinuria (5 grams/24 hours) and
fetal growth restriction as possible features of severe
disease because massive proteinuria has a poor
correlation with outcome and fetal growth restriction is
managed similarly whether or not preeclampsia is
diagnosed.
• Oliguria was removed as a characteristic of severe
disease.
• PREVALENCE — Preeclampsia is estimated to
occur in 4.6 percent of pregnancies
worldwide. 1.5-fold to 2-fold higher in first
pregnancies
RISK FACTORS
●A past history of preeclampsia increases the risk of developing
preeclampsia in a subsequent pregnancy seven-fold compared to women
without this history
The severity of preeclampsia strongly impacts this risk. Women with
severe features of preeclampsia in the second trimester are at greatest
risk of developing preeclampsia in a subsequent pregnancy: rates of 25 to
65 percent have been reported . By comparison, women without severe
features of preeclampsia in their first pregnancy develop preeclampsia in 5
to 7 percent of second pregnancies. Women who had a normotensive first
delivery develop preeclampsia in less than 1 percent of second
pregnancies.
●First pregnancy (nulliparity) ..
●A family history of preeclampsia in a first degree suggesting a
heritable mechanism in some cases
• Preexisting medical conditions:
•Pregestational diabete:
•Blood pressure ≥130/80 mm Hg.
•Antiphospholipid antibodies SYN.
•Body mass index ≥26.1
•Chronic kidney disease (CKD)
●Twin pregnancies
●Advanced maternal age
• Of note, women who smoke cigarettes have a lower risk of
preeclampsia than nonsmokers
• CLINICAL MANIFESTATIONS
Signs and symptoms:
●Severe hypertension (systolic blood pressure ≥160 mm Hg or diastolic
≥110 mm Hg on two occasions at least four hours apart or only
once if treated)
●Persistent and/or severe headache
●Visual abnormalities (scotomata, photophobia, blurred vision, or
temporary blindness [rare])
●Upper abdominal or epigastric pain
●Nausea, vomiting
●Dyspnea, retrosternal chest pain
●Altered mental status
Laboratory abnormalities:
●Microangiopathic hemolytic anemia (abnormal peripheral smear,
elevated bilirubin, or low serum haptoglobin levels U/L)
●Thrombocytopenia (<100,000/microL)
●Elevated serum creatinine concentration (>1.1 mg/dL)
●Elevated liver enzymes (twice the upper limit of normal)
• Atypical presentation —
●Onset of signs/symptoms at <20 weeks of
gestation
●Hypertension or proteinuria (but not both)
with or without characteristic signs and
symptoms of severe preeclampsia
●Delayed postpartum onset or exacerbation of
disease (>2 days postpartum)
Preeclampsia: Pathogenesis

Development abnormalities of the uteroplacental circulation occur
long before clinical manifestations of preeclampsia become evident.
In preeclampsia, the cytotrophoblast infiltrates the decidual portion
of the spiral arteries, but fails to penetrate the myometrial portion.
Thus, the large, tortuous vascular channels characteristic of the
normal placenta do not develop; instead, the vessels remain narrow,
resulting in hypoperfusion.
 The focus on immunologic factors as a possible contributor to the
placental abnormality is based, in part, upon the observation that
prior exposure to paternal/fetal antigens appears to protect against
preeclampsia.
 Both maternal and paternal contributions to fetal genes may have a
role in defective placentation and subsequent preeclampsia. In
particular, a genetic locus on chromosome 13 appears to be
associated with development of preeclampsia and may be
responsible for the production of circulating anti-endothelial factors.
Preeclampsia: Pathogenesis
 The ischemic placenta appears to elaborate factors into the
maternal bloodstream that alter maternal endothelial cell
function and lead to the characteristic systemic signs and
symptoms of preeclampsia. Many of the clinical features of
preeclampsia can be explained as clinical responses to
generalized endothelial dysfunction.
 Soluble fms–like tyrosine kinase 1 (sFlt-1) is a circulating
antagonist to vascular endothelial growth factor (VEGF). It is
released by the diseased placenta and is an important
mediator of the maternal signs and symptoms of
preeclampsia.
Prediction of preeclampsia
●Multiple risk factors for development of preeclampsia have been described .
However, most of these risk factors are not highly predictive of the disorder,
nor are they modifiable.
●No clinically available tests perform well in distinguishing women who will
develop preeclampsia from those who will not. Use of these tests has not
been proven to improve pregnancy outcome.
●Measurement of angiogenic factors (VEGF, PlGF, sFlt-1, sEng) in blood or
urine is the most promising approach for predicting preeclampsia; however,
these tests are investigational and are not available for clinical use at
present. The ratio of sFlt-1:VEGF (or sFlt-1:PlGF), rather than absolute levels
of these factors, appears to be most useful.
All pregnant women should be assessed for and educated about the signs and
symptoms of the disease. We recommend not using laboratory or imaging
tests to screen for preeclampsia
Preeclampsia: Prevention
 Low-dose aspirin is the only drug for which there is some evidence
of benefit in reducing the risk of preeclampsia.
 For women at low-risk for development of preeclampsia, we
recommend avoiding low-dose aspirin There is no evidence of
benefit.
 For women at moderate to high risk of developing preeclampsia,
we suggest low-dose aspirin prophylaxis . A modest reduction in the
risk of preeclampsia and its sequelae (growth restriction, preterm
birth) is possible. There are no validated methods (biomarkers,
clinical diagnostic tests, medical history) for identifying women at
high risk for preeclampsia.
The optimum low dose of aspirin is unclear; we suggest 81 mg per
day , beginning at the end of the first trimester. Aspirin is
discontinued 5 to 10 days before expected delivery to diminish the
risk of bleeding during delivery; however, no adverse maternal or
fetal effects related to low-dose aspirin have been proven.
Preeclampsia: Prevention
 ●We do not recommend routine calcium supplementation above
the recommended daily allowance for healthy, nulliparous women
to prevent preeclampsia . There may be a benefit for preeclampsia
prevention in high-risk populations or in those consuming a low
calcium diet. The recommended daily allowance for elemental
calcium is 1000 mg per day in pregnant and lactating women 19 to
50 years of age (1300 mg for girls 14 to 18 years old).
 ●We do not recommend vitamin C and E supplementation to
prevent preeclampsia
 ●We do not recommend fish oil for preventing preeclampsia
 ●No drug prevents progression to more severe disease.
 ●We suggest not restricting salt intake or activity for primary
prevention of preeclampsia or progression of disease . However,
reduced physical activity may be useful for improving uterine blood
flow in pregnancies with fetal growth restriction, and may be a
useful adjunct to antihypertensive therapy in women with high
blood pressure.
Management and prognosis
•
•
The definitive treatment of preeclampsia is delivery: to prevent development of
maternal or fetal complications from disease progression.
Timing of delivery is based upon gestational age, the severity of preeclampsia, and
maternal and fetal condition
• APPROACH BASED ON DISEASE SEVERITY:
• Preeclampsia with features of severe disease : is generally regarded as an
indication for delivery in the following settings:
Before fetal viability
At ≤34 weeks of gestation
When the maternal or fetal condition is unstable
. Cervical ripening agents can be used prior to induction if the cervix is not favorable
However, we feel that a prolonged induction and inductions with a low likelihood of
success are best avoided. Cesarean delivery is reasonable for women with severe
preeclampsia/eclampsia who are under about 32 weeks of gestation and have a low
Bishop score, given the high frequency of nonreassuring fetal heart rate tracings and
failure of the cervix to dilate in this setting .
Preeclampsia without features of severe
disease
• For women with preeclampsia without features of
severe disease, we suggest expectant management
with delivery at ≥37 weeks of gestation
• Experts consistently recommend delivery of women
with preeclampsia at ≥37 weeks of gestation, even in
the absence of features of severe disease (previously
called “mild preeclampsia”) Cervical ripening agents
should be used in women with unfavorable cervices.
EXPECTANT ANTEPARTUM MANAGEMENT OF PREECLAMPSIA
WITHOUT FEATURES OF SEVERE DISEASE
• consists of frequent laboratory monitoring (platelet count, liver and renal
function tests), assessment of maternal blood pressure and symptoms,
and evaluation of fetal growth and well-being. In most patients,
antihypertensive therapy is not indicated for systolic blood pressure <160
mmHg or diastolic blood pressure <110 mmHg
• For women with a viable fetus and preeclampsia <34 weeks of gestation,
we recommend a course of antenatal glucocorticoids (betamethasone) .
• For women with preeclampsia and features of severe disease, we
recommend intrapartum and postpartum seizure prophylaxis
. The benefit of seizure prophylaxis is less clear in women without severe
hypertension or preeclampsia symptoms; however, we also suggest
intrapartum and postpartum prophylaxis for these women .
We recommend the use of magnesium sulfate as a first-line agent for
seizure prophylaxis in preeclampsia
Inpatient versus outpatient care
• Restricted activity may be recommended since blood pressure is lower in
rested patients; however, there is no evidence that bedrest improves
pregnancy outcome or delays progression of disease.
• bedrest in the hospital increases the risk of venous thromboembolism .
• Rest in the left lateral decubitus position can augment uteroplacental flow,
which may benefit some pregnancies.
• If signs or symptoms of disease progression are noted, hospitalization for
more intensive monitoring and possible delivery is indicated.
• Outpatients should be aware of the signs and symptoms of preeclampsia
and they should monitor fetal movements daily .
• They should be told to call their healthcare provider immediately if they
develop severe or persistent headache, visual changes, shortness of
breath, or right upper quadrant or epigastric pain.
• Laboratory follow-up :— The minimum laboratory evaluation should
include platelet count, serum creatinine, and liver enzymes. These tests
should be repeated at least weekly in women with nonsevere
preeclampsia to assess for disease progression, and more often if clinical
signs and symptoms suggest worsening disease .
• The value of other tests is less clearly defined. A rising hematocrit can be
useful to look for hemoconcentration, which suggests contraction of
intravascular volume and progression to more severe disease, while a
falling hematocrit may be a sign of hemolysis. An elevated serum indirect
bilirubin concentration is a better sign of hemolysis, although an elevated
LDH may also be a marker of severe disease or HELLP syndrome.
Hemolysis can be confirmed by observation of schistocytes and helmet
cells on a blood smear
• repeated 24-hour urinary protein estimations are not useful once the
threshold of 300 mg/24 hours or protein/creatinine ratio ≥0.3
mg/dL/mg/dL for the diagnosis of preeclampsia has been exceeded.
Serum creatinine alone can be used to monitor renal function.
• Treatment of hypertension :
• Blood pressure should be assessed at least twice weekly. The
use of antihypertensive drugs to control mild hypertension in
the setting of preeclampsia does not alter the course of the
disease or diminish perinatal morbidity or mortality, and
should be avoided in most patients.
• Sodium restriction below the recommended daily intake and
diuretics have no role in routine therapy .
• Although intravascular volume is reduced, a randomized trial
showed that plasma volume expansion did not improve
maternal or fetal outcome
• Assessment of fetal well-being :
• daily fetal movement counts
• twice weekly fetal nonstress testing
• with assessment of amniotic fluid volume, or twice weekly
biophysical profiles.
• Testing is repeated immediately if there is an abrupt change
in maternal condition.
• Evaluation of umbilical artery Doppler indices is also useful,
as the results help in optimal timing of delivery.
• The frequency of assessment depends on the findings;
weekly assessment is reasonable when Doppler indices are
normal.
• Assessment of fetal growth
• Early fetal growth restriction may be the first
manifestation of preeclampsia and is a sign of severe
uteroplacental insufficiency.
• We suggest performing sonographic estimation of fetal
weight to evaluate for growth restriction and
oligohydramnios at the time of diagnosis of
preeclampsia.
• If the initial examination is normal, we repeat the
ultrasound examination every three weeks. Management
of the growth restricted fetus is reviewed separately.
Antenatal corticosteroids :
•
•
Although preeclampsia may accelerate fetal lung
maturation, neonatal respiratory distress remains common
in premature neonates of preeclamptic pregnancies .
Antenatal corticosteroids (betamethasone) to promote
fetal lung maturity should be administered to women <34
weeks of gestation since they are at increased risk of
progression to severe disease and preterm delivery
INTRAPARTUM MANAGEMENT
• Intrapartum monitoring :
• Continuous maternal-fetal monitoring is indicated intrapartum to identify
worsening hypertension, deteriorating maternal hepatic, renal, cardiopulmonary,
neurological, or hematologic function, as well as abruptio placentae or a
nonreassuring fetal heart rate tracing
• Fluids — Fluid balance should be monitored closely to avoid excessive
administration, since women with severe disease are at risk of pulmonary edema
and significant third-spacing. Maintenance fluids of 80 mL/hour are often
adequate in the absence of ongoing fluid loss, such as bleeding. Oliguria that
does not respond to a modest trial of increased fluids should be tolerated.
Diuretics are only indicated for treatment of pulmonary edema.
• Management of hypertension — Severe hypertension in labor should be treated
with intravenous labetalol or hydralazine or oral nifedipine to prevent stroke.
Antihypertensive medications do not prevent eclampsia.
• Invasive hemodynamic monitoring :
•
Although not routinely recommended even in the setting of
severe preeclampsia, invasive hemodynamic monitoring can be
useful in complicated patients, such as those with severe
cardiac disease, severe renal disease, severe oliguria, refractory
hypertension, or pulmonary edema.
•
However, most women can be managed without these tools
and should not be exposed to the risks associated with arterial
and central venous catheterization.
• Seizure prophylaxis :
• we administer intrapartum and postpartum
magnesium sulfate seizure prophylaxis to all
women with preeclampsia.
• We do not administer seizure prophylaxis to
women with only gestational hypertension
(pregnancy-related hypertension without
proteinuria or end-organ dysfunction), as the
seizure risk in the latter group is less than 0.1
percent
• Magnesium sulfate versus other
anticonvulsants:
Major medical organizations worldwide
consistently recommend magnesium sulfate
as the drug of choice for the prevention of
eclampsia
• In meta-analyses of randomized trials in
eclamptic women, magnesium sulfate was
safer and more effective for prevention of
recurrent seizures than phenytoin, diazepam
• Magnesium regimen and monitoring:
• —The drug is usually initiated at the onset of labor or induction, or
prior to a cesarean delivery . Prolonged antepartum therapy (more
than five to seven days) in women with preterm labor has been
associated with adverse effects on fetal bones.
• Dosing — Although published dosage regimens for magnesium sulfate
vary widely (loading dose of 4 to 6 grams intravenously and
maintenance dose of 1 to 3 grams per hour), the most common
regimen, and the one that we use, is a loading dose of 6 grams
intravenously over 15 to 20 minutes followed by 2 grams per hour as a
continuous infusion .
• An alternative regimen is 5 grams intramuscularly into each buttock
(total of 10 grams) followed by 5 grams intramuscularly every four
hours. However, this method is associated with more side effects,
particularly pain at the injection site.
• There does not appear to be a clear threshold concentration for
insuring the prevention of convulsions, although a therapeutic range of
4.8 to 8.4 mg/dL (2.0 to 3.5 mmol/L)
• Since magnesium sulfate is excreted by the kidneys, dosing
should be adjusted in women with renal insufficiency (defined
as a serum creatinine greater than 1.0 mg/dL). Such women
should receive a standard loading dose (since their volume of
distribution is not altered), but a reduced maintenance dose (1
gram per hour or no maintenance dose if the serum creatinine
is greater than 2.5 mg/dL) and close monitoring of their serum
magnesium level every six hours or by clinical assessment every
one to two hours.
• The maintenance phase is given only if a patellar reflex is
present (loss of reflexes being the first manifestation of
symptomatic hypermagnesemia), respirations exceed 12 per
minute, and the urine output exceeds 100 mL per four hours.
• Duration of therapy:
• Magnesium sulfate is usually continued for 24
hours postpartum
• In women who have nonsevere preeclampsia,
discontinuation of therapy after 12 hours may be
safe .
• In women with severe preeclampsia or eclampsia,
seizure prophylaxis is generally continued for 24 to
48 hours postpartum, after which the risk of
recurrent seizures is low.
• Diuresis (greater than 4 L/day) is believed to be
the most accurate clinical indicator of resolution of
preeclampsia/eclampsia.
• Complications and side effects :
• — Rapid infusion of magnesium sulfate causes diaphoresis,
flushing, and warmth, probably related to peripheral
vasodilation . Nausea, vomiting, headache, muscle weakness,
visual disturbances, and palpitations can also occur. Dyspnea or
chest pain may be symptoms of pulmonary edema, which is a
rare side
• Toxicity is related to serum magnesium concentration:
• loss of deep tendon reflexes occurs at 9.6 to 12.0 mg/dL
• respiratory paralysis at 12.0 to 18.0 mg/dL
• cardiac arrest at 24 to 30 mg/dL
• Calcium gluconate (1 gram intravenously over 5 to 10 minutes)
should be administered only to counteract life-threatening
symptoms of magnesium toxicity (such as cardiorespiratory
compromise).
• Magnesium sulfate is contraindicated in women with
myasthenia gravis since it can precipitate a severe myasthenic
crisis
• POSTPARTUM MANAGEMENT :
• — Nonsteroidal antiinflammatory drugs (NSAIDs) for pain control
should be avoided in women with poorly controlled hypertension,
oliguria, renal insufficiency, or thrombocytopenia.
• We monitor vital signs every two hours while the patient remains on
magnesium sulfate and we repeat laboratory tests until two
consecutive sets of data are normal.
• Severe hypertension should be treated; some patients will have to be
discharged on antihypertensive medications, which are discontinued
when blood pressure returns to normal.
• The American College of Obstetricians and Gynecologists suggests
monitoring blood pressure in hospital or at home for the first 72 hours
postpartum and again 7 to 10 days post-delivery.
• Some patients will require longer monitoring; continued follow-up is
needed until all of the signs and symptoms of preeclampsia have
resolved.
• Postpartum onset of preeclampsia:
• In women who are initially diagnosed with preeclampsia after
delivery, magnesium sulfate should be administered to those
at increased risk of developing seizures
• Women with new onset hypertension and headache or
blurred vision, or Women with severe hypertension
Antihypertensive therapy should also be initiated. The
American College of Obstetricians and Gynecologists suggests
treatment of systolic blood pressure ≥150 mmHg or diastolic
blood pressure ≥100 mmHg on two occasions four to six hours
apart .
• Indications for antihypertensive
therapy:
• — We do not prescribe antihypertensive
therapy for mild hypertension, which we define
as blood pressures consistently less than
150/100 mmHg. The only benefit that has been
demonstrated so far of antihypertensive therapy
in pregnant women with mild hypertension is a
reduction in risk of developing severe
hypertension
• Severe hypertension should be treated to prevent
maternal vascular complications (eg, stroke, heart failure).
• There is no consensus as to the optimal blood pressure
threshold for initiating therapy. We initiate
antihypertensive therapy in adult women at systolic
pressures ≥150 mmHg or diastolic blood pressures ≥100
mmHg.
• Other physicians begin antihypertensive treatment when
systolic pressure is ≥160 mmHg or diastolic pressure is
≥105 to 110 mmHg .
• Choice of drug and dose:
• There are two settings in which antihypertensive
therapy is used in preeclampsia:
• Acute management of severe hypertension,
which may require parenteral therapy
• Longer-term blood pressure control during
expectant management of severe preeclampsia
• Acute therapy:
• — We suggest labetalol or hydralazine as first-line agents for acute
therapy of severe hypertension., but nimodipine, diazoxide, and
ketanserin were probably best avoided.
• ●Labetalol – We recommend intravenous labetalol for first-line
therapy because it is effective, has a rapid onset of action, and a
good safety profile.
Begin with 20 mg intravenously over 2 minutes followed at 10minute intervals by doses of 20 to 80 mg up to a maximum total
cumulative dose of 300 mg. As an example, give 20 mg, then 40 mg,
then 80 mg, then 80 mg, then 80 mg.
• ●Hydralazine – Begin with 5 mg intravenously over 1 to 2 minutes; if
the blood pressure goal is not achieved within 20 minutes, give a 5 to
10 mg bolus depending upon the initial response. The maximum
bolus dose is 20 mg. If a total dose of 30 mg does not achieve
optimal blood pressure control, another agent should be used.
• Calcium channel blockers – Sustained release
nifedipine (30 mg) and immediate release
nicardipine are other options. Nicardipine can
be given intravenously.
If used, a common dose for nifedipine is 10
mg orally administered at 20-minute intervals
until the target blood pressure is achieved.
• Nitroglycerin – Nitroglycerin (glyceryl
trinitrate) is a good option for treatment of
hypertension associated with pulmonary
edema
• Drugs to avoid in pregnancy
• ACE inhibitors, ARBs, direct renin inhibitors
• Nitroprusside
• PROGNOSIS:
•
— Prognostic issues include the risk of recurrent
preeclampsia and related complications in subsequent
pregnancies and long-term maternal health risks.
• Recurrence — The recurrence risk varies with the
severity and time of onset of the acute episode .
• Women with early onset, severe preeclampsia are at
greatest risk of recurrence (as high as 25 to 65 percent)
.
• The risk is much lower (5 to 7 percent) in women who
had nonsevere preeclampsia during the first pregnancy,
versus less than 1 percent in women who had a
normotensive first pregnancy (does not apply to
abortions) .
• Management — Antihypertensive agents may be
required temporarily postpartum if hypertension is
severe.
• We recommend initiating therapy if blood pressures
are persistently greater than 140 mm Hg systolic at the
time of discharge from the hospital. Oral medications
similar to those used in the nonpregnant population
can be prescribed, with modifications if the woman is
breastfeeding.
• Brief furosemide therapy (20 mg orally once or twice
per day for five days) may facilitate return to
normotension in women with severe, but not mild,
preeclampsia, particularly those with significant edema
One guideline suggests avoiding methyldopa
postpartum because of the risk of postnatal depression